Histological grading and staging in chronic hepatitis: clinical applications and problems |
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Authors: | SG Hübscher |
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Affiliation: | LSU Medical Center, Department of Molecular and Cellular Physiology, Shreveport, LA 71130, USA. |
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Abstract: | Exposure of endothelial monolayers to hydrogen peroxide results in increased solute permeability in a time- and dose-dependent fashion. This effect is prevented by either staurosporine, an inhibitor of PKC, or by G?6976, an inhibitor of "classical" PKC isoforms. Immunohistochemistry of peroxide-treated monolayers illustrates a loss of cadherin staining at cell junctions and gap formation predominantly at tri-cellular junctions. Both staurosporine and G?6976 prevented peroxide-induced gap formation. Peroxide also stimulated internalization of cadherins as measured by the trypsin protection assay, which was not blocked by staurosporine or G?6976. These data suggest that peroxide causes: 1) a time- and dose-dependent increase in permeability and dose-dependent increase in gap formation, both of which are PKC dependent; and 2) promotes PKC-independent cadherin internalization. These data indicate that cadherin internalization may be part of the mechanism through which oxidants regulate solute permeability. |
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